A study has been made of arterial blood changes during the respiratory cycle in patients with cardiac enlargement, prolonged circulation time, and Cheyne-Stokes breathing. In these patients, Cheyne-Stokes breathing appeared to depend upon the delay in passage of blood from the lungs to the arterial chemoreceptors and respiratory center. This delayallowed cyclic over- and underventilation. There was little or no central nervous system depression. In contrast, one case of Biot's breathing is presented as an example of another mechanism responsible for periodic breathing. Here irregular breathing seems to depend on fluctuations in activity of a severely damaged central nervous system.

Reflex venomotor activity has been observed and measured in normal subjects by means

The arterial pressure is kept at a nearly constant level in normal man by simultaneous adjustments of the cardiac output and calibre of the arterioles. The normal response on motionless standing is arteriolar constriction and a moderate fall in cardiac output. The arteriolar constriction is usually sufficient to prevent a fall in mean pressure. In certain persons a marked fall in arterial pressure occurs on motionless standing. The purpose of this study is to evaluate the relative importance of an abnormal decline in cardiac output and of a failure of normal vasoconstriction in producing the fall in arterial pressure. METHODSAmong the 12 patients studied, postural hypotension was idiopathic in three, associated with diabetes mellitus in five, with tabes dorsalis in two, with probable syringomyelia in one, and followed bilateral sympathectomy (T. through LJ) for hypertension in one case.3 All subjects were studied in the morning, usually after a light breakfast. Observations were made on a tilting table in the supine position, and at a foot-down angle which was usually 60°from the horizontal. In the latter position the patient was supported by a foot-plate. The tilted position was maintained for three to four minutes before beginning air collection for determination of oxygen c6n-sumption. The air collection usually occupied two minutes, and toward the end of this time blood samples were drawn and pressure measurements were begun. The total duration of tilt was seven to eight minutes. The time allowed for adjustment to the tilted position is therefore quite short. However, if more time is allowed to reach a steady state during the tilt, there is danger of collapse. None of these subjects showed evidence of impending collapse. In one subject (J. D.) A-V blood oxygen differences were determined three minutes apart during the tilt, and in two subjects (C. G. and J. P.) duplicate venous samples were taken approximately one minute apart (before and after drawing the arterial sample). The results, presented in Table I, do not indicate rapid shifts in A-V oxygen difference during the period of measurement.Albumin infusion consisted of 75 gm. of human serum albumin4 made up with normal saline to a volume of 1,300 cc. and given intravenously within a period of 15 minutes.Cardiac outputs were determined by the Fick principle following intracardiac catheterization (1). Mixed venous blood was obtained from the atrium or the pulmonary artery; arterial blood, from the brachial artery through an inlying needle. Blood oxygen contents were determined by a spectrophotometric method (2) or by the method of Van Slyke and Plazin (3). In the latter case, duplicate analyses were required to check within 0.1 vol. %. With the spectrophotometric method, duplicate determinations are not in general done because of the simplicity of the technique. Repeated determinations of arterio-venous oxygen difference on the same blood samples yield results within 0.2 vol. %, unless the hemolyzed samples are grossly turbid. All samples are checked for t...

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SUMMARY. The present study evaluates the transitional or border zone of intermediate blood flow reduction between nonischemic and ischemic regions after acute coronary artery occlusion in chronically instrumented dogs, using methods that minimize an admixture of ischemic and nonischemic myocardium in the tissue analyzed. The regions perfused by occluded and nonoccluded vessels were identified by tracing the extra and intramural distribution of the coronary vasculature from postmortem angiograms. Regional blood flow was evaluated in serial 3-mm-wide epicardial and endocardial zones from outside and inside the interface between occluded and nonoccluded vessels. The zone of intermediate reduction in blood flow between nonischemic and ischemic regions occurred in the first 3-mm section immediately inside the region supplied by the occluded vasculature. Mean blood flow in this region was reduced to 58 ± 6% and 61 ± 5% (±SEM) of nonischemic region blood flow at the lateral and medial epicardial margins, respectively, and 47 ± 5% and 45 ± 6% at the lateral and medial endocardial margins, respectively. In the remaining ischemic zone, significant differences in blood flow existed between epicardial and endocardial layers; these differences were highly variable between animals. The data indicate that when the analysis of regional blood flow following acute ischemia is based on the anatomic distribution of the coronary vasculature, the transitional or border zone of intermediate reduction in blood flow is limited to a narrow zone immediately inside the occluded vasculature. Studies performed in acutely anesthetized dogs in which the occluded region was perfused via a two-chamber blood reservoir that allowed maintenance of perfusion and exclusion of microspheres from the circumflex region indicate that intermediate reductions in blood flow at the border of the ischemic zone resulted from an admixture of normal myocardium and, thus, do not represent a border zone of intermediate ischemia.